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148 Cards in this Set
- Front
- Back
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Potassium
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The major cation in intracellular fluid
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Potassium
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Vital for skeletal, cardiac and smooth muscle transmission and conduction.
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Sodium
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The major cation in extracellular fluid
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Sodium
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Is important in controlling and regulating water balance
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Intracellular
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The fluid within the cell
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Extracellular
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The fluid outside the cell
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Intravascular
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The fluid or plasma found in the blood vessel
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Interstitial
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The fluid that surrounds the cell
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Transcellular
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The fluid enclosed by a epithelial membrane
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Dysfunction or trauma can cause
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-Decreased amount of water in body
-Increased amount of Na+ in the body -Increased blood osmolality -Decreased circulating blood volume |
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Edema
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is the accumulation of fluid within the interstitial spaces.
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Edema causes:
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-increased hydrostatic pressure
-lowered plasma osmotic pressure -increased capillary membrane permeability -lymphatic channel obstruction |
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Renal tubule reabsorption affected by hormones:
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-Aldosterone
-Renin/angiotensin -Atrial Natriuretic Peptide -(ANP) |
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Hypernatremia
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-Water moves from ICF → ECF
-Cells dehydrate Due to ↑ Na + or ↓ water |
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Clinical manifestations of Hypernatremia
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-Thirst
-Lethargy -Neurological dysfunction due to dehydration of brain cells -Decreased vascular volume |
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Treatment of Hypernatremia
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Lower serum Na+
-Isotonic salt-free IV fluid -Oral solutions preferable |
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Hyponatremia
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Overall decrease in Na+ in ECF
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Na+ loss results from...
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-diuretics, chronic vomiting
-Chronic diarrhea -Decreased aldosterone -Decreased Na+ intake |
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Clinical manifestations of Hyponatremia
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Neurological symptoms
-Lethargy, headache, confusion, apprehension, depressed reflexes, seizures and coma Muscle symptoms -Cramps, weakness, fatigue Gastrointestinal symptoms -Nausea, vomiting, abdominal cramps, and diarrhea Tx – limit water intake or discontinue meds |
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Hypokalemia
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Serum K+ < 3.5 mEq /L
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Hypokalemia with diabetes...
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-Insulin gets K+ into cell
-Ketoacidosis – H+ replaces K+, which is lost in urine |
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Causes of Hypokalemia
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-Decreased intake of K+
-Increased K+ loss ---Chronic diuretics ---Acid/base imbalance ---Trauma and stress ---Increased aldosterone ---Redistribution between ICF and ECF |
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Clinical manifestations of Hypokalemia
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-Neuromuscular disorders
Weakness, flaccid paralysis, respiratory arrest, constipation -Dysrhythmias, appearance of U wave -Postural hypotension -Cardiac arrest |
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Hyperkalemia
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-Check for renal disease
-Massive cellular trauma -Insulin deficiency -Addison’s disease -Potassium sparing diuretics -Decreased blood pH -Exercise causes K+ to move out of cells |
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Early Clinical manifestations of Hyperkalemia
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hyperactive muscles , paresthesia
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Late Clinical manifestations of Hyperkalemia
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-Muscle weakness, flaccid paralysis
-Change in ECG pattern -Dysrhythmias -Bradycardia , heart block, cardiac arrest |
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Treatment Hypokalemia
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Increase K+ intake, but slowly, preferably by foods
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Treatment of Hyperkalemia
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-If time, decrease intake and increase renal excretion
-Insulin + glucose -Bicarbonate -Ca++ counters effect on hear |
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Calcitonin
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-Promotes bone formation
-↑ renal excretion |
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Hypercalcemia Results from:
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-Hyperparathyroidism
-Hypothyroid states -Renal disease -Excessive intake of vitamin D Milk-alkali syndrome -Certain drugs -Malignant tumors |
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Hypercalcemia effects:
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-Many nonspecific – fatigue, weakness, lethargy
-Increases formation of kidney stones and pancreatic stones -Muscle cramps -Bradycardia, cardiac arrest -Pain GI activity also common ---Nausea, abdominal cramps ---Diarrhea / constipation -Metastatic calcification |
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Hypocalcemia
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-Hyperactive neuromuscular reflexes and tetany
-Convulsions in severe cases |
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Hypocalcemia caused by:
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-Renal failure
-Lack of vitamin D -Suppression of parathyroid function -Hypersecretion of calcitonin -Malabsorption states -Abnormal intestinal acidity and acid/ base bal. -Widespread infection or peritoneal inflammation |
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Hypocalcemia diagnosis
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-Chvostek’s sign
-Trousseau’s sign |
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Hypocalcemia treatment:
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-IV calcium for acute
-Oral calcium and vitamin D for chronic |
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60% of a patient’s body weight
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Body Water
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Cations
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Sodium 135 - 145
Potassium 3.5 - 4.5 Calcium 4.0 - 5.5 Magnesium 1.5 - 2.5 |
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Anions
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Chloride 95 - 105
CO2 24 - 30 phosphate 2.5 - 4.5 |
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Aldosterone
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-distal tubules
-sodium exchanged for K+ and H+ -released by volume reduction |
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Antidiuretic Hormone (ADH)
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-increased tubular water reabsorption
-posterior pituitary release |
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Acidosis
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pH < 7.2
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Acidosis s/e
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-decreased responsiveness to catecholamines
-cardiac dysfunction arrhythmias -increased potassium serum levels |
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to Correct sodium to above 120 mEq/dl
(hyponatremia) |
-NaCl + 40 mEq/L KCl
-3% Saline -furosemide diuresis (euvolemic) -serial electrolytes -be prepared to handle seizure |
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S/S Hyponatremia
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-Seizures, coma, encephalopathy
-Results from rapid [Na] -Cramping, twitches, fasciculations -Results from ion conduction aberrations |
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Treatment for HYPERKALEMIA
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-CaCl2 10% - 1 ampule
-Sodium Bicarbonate - 1 ampule -D50 & Insulin 10 U 2 - agonist nebulizer- cellular K -Kayexalate® |
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Causes of Hyperkalemia
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-Renal dysfunction
-Acidemia -Hypoaldosteronism Drugs -Excessive intake -WBC > 100,000 -Platelets > 600,000 |
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Causes of Hyperkalemia
--Cell Death |
-Rhabdomyolysis
-Tumor lysis -Burns -Hemolysis |
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Hypomagnesemia
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Mg< 1.6 mg/dL
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Hypomagnesemia causes...
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poor diet, diuretics, gut losses, & massive diarrhea, resuscitation.
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DIABETES INSIPIDUS
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[Na+] >150
-Urine specific gravity 1.007 polyuria, clear urine |
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Treatment
DIABETES INSIPIDUS |
free water deficit
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HYPOPHOSPHATEMIA
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“Refeeding Syndrome”
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“Refeeding Syndrome”
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malnutrition
alcoholism |
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Hypermagnesemia s/s
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-Prolonged PR interval
-Hypotension, hyporeflexia, paralysis |
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Treatment
Hypermagnesemia |
-Calcium gluconate
-Normal saline -Loop diuretics -dialysis |
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A blood pH of 7.6 would indicate:
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alkalosis
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Alkalosis
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Blood pH above normal (greater than 7.45 in arterial blood). It can be either metabolic (bicarbonate excess) or respiratory (carbonic acid deficit)
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HYPOTONIC
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Solutions move into cells causing them to enlarge
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HYPERTONIC
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Solutions pull fluid from cells
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Creatinine
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end product of muscle metabolism; better indicator of renal function
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Creatinine levels
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0.7-1.5 mg/dL
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HYDROSTATIC PRESSURE
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“Fluid- pushing pressure inside a capillary”*
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RENIN
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release aldosterone & causes an increase in peripheral vasoconstriction
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Dehydration
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May be treated with hypotonic sol (like dextrose 5% in water)
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FLUID VOLUME DEFICIT
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increase in heart rate & cardiac contraction; thirst; plus release of ADH & aldosterone
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CAUSES OF FVD
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-Abnormal GI fluid loss
-Abnormal fluid loss from skin -Increased water vapor from the lungs -increase renal excretion of fluids -Decrease in fluid intake -Third-space shift |
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URINE SPECIFIC GRAVITY
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1.010*-1.025*
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SIGNS & SYMPTOMS OF FVD
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-Dry mucous membranes
-Weight loss -Orthostatic hypotension & increase in pulse rate -Body temperature usually subnormal -Flat neck veins & decrease in CVP -Decreased urinary output & altered sensorium |
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NURSING MANAGEMEMT OF FVD
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-Monitoring I&O
-If urine output is below 30 mL / hr. notify the physician -Weigh patient daily -Monitor skin turgor, oral membranes, lab |
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FLUID VOLUME EXCESS
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-Hypervolemia or FVE
-increase in total sodium content -Kidney receives signal to save sodium & water -dec.:hematocrit, serum Na, serum osmolality, urine sp. Gr; inc. BUN |
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SIGNS & SYMPTOMS OF FVE
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-SOB & orthopnea
-Edema & weight gain -Distended neck veins & tachycardia -Increased blood pressure -Crackles & wheezes -Maybe ascites & pleural effusion -Increase in CVP |
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NURSING MANAGEMENT OF FVE
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-Monitor I & O
-Check for edema & weigh patient daily -Restrict sodium intake as prescribed -Limit intake of fluids -Watch for signs of potassium imbalance -Monitor for signs of pulmonary edema -Place patient in semi-Fowler’s position |
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ISOTONIC SOLUTIONS
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-0.9% Sodium Chloride Solution
-Ringer’s Solution -Lactated Ringer’s Solution |
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HYPOTONIC SOLUTIONS
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-5% DEXTROSE & WATER
-0.45% SODIUM CHLORIDE -0.33% SODIUM CHLORIDE |
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HYPERTONIC SOLUTIONS
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-3% SODIUM CHLORIDE
-5% SODIUM CHLORIDE -WHOLE BLOOD -ALBUMIN -TOTAL PARENTERAL NUTRITION -TUBE FEEDINGS -CONCENTRATED DEXTROSE (>10%) |
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CHIEF BASE OF BLOOD
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SODIUM (NA+)
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The thirsty person will not get this !!!!
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HYPERNATREMIA
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HYPERNATREMIA
IV solutions given |
infusion of 0.45% NaCl
gradually lower serum sodium |
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HYPONATREMIA
iv solutions given |
infusing isotonic saline
seeks to correct cause & give sodium with caution due to possible rebound fluid excess |
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PRIMARY BUFFER IN CELL
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POTASSIUM (K+)
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Major cause is renal disease
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HYPERKALEMIA
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pseudohyperkalemia
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prolonged tourniquet, hemolysis of blood, sampling above KCl infusion
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EKG shows tall, peaked T waves & dysrthythmias
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HYPERKALEMIA
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cause is increase renal loss most often associated with diuretics
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HYPOKALEMIA
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Can increase the action of digitalis
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HYPOKALEMIA
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HYPOKALEMIA TX
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Oral or IV administration of potassium
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Respiratory Acidosis
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-pH < 7.35
-PaCO2 > 45mm Hg -Due to inadequate alveolar ventilation |
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Respiratory Alkalosis
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-pH > 7.45
-PaCO2 < 35mm Hg -Due to alveolar hyperventilation & hypocapnia |
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Metabolic Acidosis
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-pH < 7.35
-HCO3 < 22mEq/L -Due to gain of acids or loss of base (like excessive GI loss from diarrhea) -May have associated hyperkalemia |
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Metabolic Alkalosis
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-pH > 7.45
-HCO3 > 26 mEq/L -Due to loss of acid or gain of base (most common is vomiting or gastric suction) -Hypokalemia may produce alkalosis |
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Higher PaCO2 causes ...
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acidosis (lower pH)
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Lower PaCO2 causes...
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alkalosis (raises pH.)
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Bicarbonate (HCO3-) is a...
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base
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High HCO3- causes ...
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alkalosis (raises pH)
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Low HCO3- causes ...
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acidosis (lowers pH)
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ROME
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Respiratory Opposite
Metabolic Equal |
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< 7.35
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Acidosis
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7.35-7.45
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Normal or Compensated
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> 7.45
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Alkalosis
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Alkalosis
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High pH
High PaCO2=Metabolic Low PaCO2=Respiratory |
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Acidosis
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Low pH
High PaCO2=Respiratory Low PaCO2=Metabolic |
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If PaCO2 is abnormal and pH is normal, it indicates ...
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compensation
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Normal RBC's
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4,000-5,000
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Normal WBC's
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5,000-10,000
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Normal Platletes
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150,000-400,000
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NOrmal HCT
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40
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Normal HGB
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13
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Normal ANC (Absolute Neutrophil Count)
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1,500-8,000
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normal K+
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3.5-5.0
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Normal Na
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135-145
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Normal BUN
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6-26
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Normal Creat
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0.5-1.5
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Normal PT
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10 secs
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Normal PTT
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20-40 secs
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NOrmal INR
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1-2
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Normal GFR
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greater than 12.5 is good
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Hep Lock is ...
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100 units per ML
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Classic Hep Drip is ...
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25,000 units in 250 ML
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Lithium Ther. Levels
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0.8-1.4
( Above 2.0 = TOXIC) |
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Lidocaine Ther. Levels
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1.5-5 mcg
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Dilantin ther. level
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10-20
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Digoxin ther. Level
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0.5-0.8
(above 2.0 = TOXIC) |
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Short Acting Insulin
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Regular
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Regular Insulin Onset
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1/2 hour
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Regular insulin peak
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4 hours
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Regular insulin duration
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8 hours
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Intermediate Acting Insulin
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NPH
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Normal BGL
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70-110
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Normal A1C
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6-7
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NPH onset
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1.5 hours
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NPH peak
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12 hours
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NPH duration
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24 hours
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Mixed insulin
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70/30
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70/30 onset
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.5 hours
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70/30 peak
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12 hours
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70/30 duration
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24 hours
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Fast acting insulin
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Novolog
Humalog Lispro |
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Novolog/Humalog/Lispro Onset
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5-15 min.
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Novolog/Humalog/Lispro peak
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2 hours
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Novolog/Humalog/Lispro duration
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4 hours
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Long acting insulin
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Lantus
Ultra Lente |
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Lantus Onset
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2 hours and stays that level
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Lantus duration
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24 hours
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Lantus Peak
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no peak....stays at same level for 24 hours
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ultra lente onset
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4 hours
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ultra lente peak
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18 hours
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ultra lente duration
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36 hours
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